AustralieFrV1, PascalFrancis, Corpus, bibRecord, 003665

The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary

Identifieur interne : 003665 ( PascalFrancis/Corpus ); précédent : 003664; suivant : 003666

The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary

Auteurs : Robert J. Macfadyen ; M. Jennyfer Ng Kam Chuen ; Malcolm J. West ; Paul J. Nestel ; Adrienne C. Kirby ; Renate Schnabel ; David Sullivan ; R. John Simes ; Christine Pollicino ; Edith Lubos ; Thomas F. Münzel ; Harvey D. White ; Andrew M. Tonkin ; Christoph Bickel ; Laurence Tiret ; Stefan Blankenberg

Source :

European heart journal [ 0195-668X ] ; 2008.

RBID : Pascal:08-0183087

Descripteurs français

Pascal (Inist)
- Pathologie de l'appareil circulatoire, Athérosclérose, Séquence N terminale, Fragment, Peptide BNP, Tissu, Inhibiteur, Metalloendopeptidases, Métalloprotéinase, Niveau, Prédicteur, Facteur prédictif, Prédiction, Pronostic, Evolution, Lipide, Facteur risque, Risque, Pravastatine, Appareil circulatoire, Cardiologie.

English descriptors

KwdEn :
- Atherosclerosis, Brain natriuretic peptide, Cardiology, Cardiovascular disease, Circulatory system, Evolution, Fragment, Inhibitor, Level, Lipids, Metalloendopeptidases, Metalloproteinase, N terminal-Sequence, Pravastatin, Prediction, Predictive factor, Predictor, Prognosis, Risk, Risk factor, Tissue.

Abstract

Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.
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Format Inist (serveur)

NO :	PASCAL 08-0183087 INIST
ET :	The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary
AU :	MACFADYEN (Robert J.); NG KAM CHUEN (M. Jennyfer); WEST (Malcolm J.); NESTEL (Paul J.); KIRBY (Adrienne C.); SCHNABEL (Renate); SULLIVAN (David); SIMES (R. John); POLLICINO (Christine); LUBOS (Edith); MÜNZEL (Thomas F.); WHITE (Harvey D.); TONKIN (Andrew M.); BICKEL (Christoph); TIRET (Laurence); BLANKENBERG (Stefan)
AF :	University Department of Medicine and Department of Cardiology, City Hospital, Dudley Road/Birmingham B18 7QH/Royaume-Uni (1 aut., 2 aut.); University of Queensland/Brisbane/Australie (3 aut.); Baker Heart Research Institute/Melbourne/Australie (4 aut.); NHMRC Clinical Trials Centre, University of Sydney/Sydney/Australie (5 aut., 8 aut., 9 aut.); Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1/Mainz 55131/Allemagne (6 aut., 10 aut., 11 aut., 16 aut.); Royal Prince Alfred Hospital/Sydney/Australie (7 aut.); Green Lane Cardiovascular Service, Auckland City Hospital/Auckland/Nouvelle-Zélande (12 aut.); National Heart Foundation/Melbourne/Australie (13 aut.); Innere Abteilung, Bundeswehrzentralkrankenhaus/Koblenz/Allemagne (14 aut.); INSERM U525, Faculte de Medecin Pitie-Salpetriere/Paris/France (15 aut.)
DT :	Publication en série; Article; Commentaire; Niveau analytique
SO :	European heart journal; ISSN 0195-668X; Royaume-Uni; Da. 2008; Vol. 29; No. 7; 837-839, 923-931 [12 p.]; Bibl. 40 ref.
LA :	Anglais
EA :	Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.
CC :	002B12B01
FD :	Pathologie de l'appareil circulatoire; Athérosclérose; Séquence N terminale; Fragment; Peptide BNP; Tissu; Inhibiteur; Metalloendopeptidases; Métalloprotéinase; Niveau; Prédicteur; Facteur prédictif; Prédiction; Pronostic; Evolution; Lipide; Facteur risque; Risque; Pravastatine; Appareil circulatoire; Cardiologie
FG :	Peptidases; Hydrolases; Enzyme; Pathologie des vaisseaux sanguins
ED :	Cardiovascular disease; Atherosclerosis; N terminal-Sequence; Fragment; Brain natriuretic peptide; Tissue; Inhibitor; Metalloendopeptidases; Metalloproteinase; Level; Predictor; Predictive factor; Prediction; Prognosis; Evolution; Lipids; Risk factor; Risk; Pravastatin; Circulatory system; Cardiology
EG :	Peptidases; Hydrolases; Enzyme; Vascular disease
SD :	Aparato circulatorio patología; Ateroesclerosis; Secuencia N terminal; Fragmento; Péptido BNP; Tejido; Inhibidor; Metalloendopeptidases; Metaloproteasa; Nivel; Predictor; Factor predictivo; Predicción; Pronóstico; Evolución; Lípido; Factor riesgo; Riesgo; Pravastatina; Aparato circulatorio; Cardiología
LO :	INIST-18785.354000173673100120
ID :	08-0183087

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Pascal:08-0183087

Le document en format XML

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<author><name sortKey="Pollicino, Christine" sort="Pollicino, Christine" uniqKey="Pollicino C" first="Christine" last="Pollicino">Christine Pollicino</name>
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<author><name sortKey="Lubos, Edith" sort="Lubos, Edith" uniqKey="Lubos E" first="Edith" last="Lubos">Edith Lubos</name>
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</author>
<author><name sortKey="Munzel, Thomas F" sort="Munzel, Thomas F" uniqKey="Munzel T" first="Thomas F." last="Münzel">Thomas F. Münzel</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="White, Harvey D" sort="White, Harvey D" uniqKey="White H" first="Harvey D." last="White">Harvey D. White</name>
<affiliation><inist:fA14 i1="07"><s1>Green Lane Cardiovascular Service, Auckland City Hospital</s1>
<s2>Auckland</s2>
<s3>NZL</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tonkin, Andrew M" sort="Tonkin, Andrew M" uniqKey="Tonkin A" first="Andrew M." last="Tonkin">Andrew M. Tonkin</name>
<affiliation><inist:fA14 i1="08"><s1>National Heart Foundation</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bickel, Christoph" sort="Bickel, Christoph" uniqKey="Bickel C" first="Christoph" last="Bickel">Christoph Bickel</name>
<affiliation><inist:fA14 i1="09"><s1>Innere Abteilung, Bundeswehrzentralkrankenhaus</s1>
<s2>Koblenz</s2>
<s3>DEU</s3>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tiret, Laurence" sort="Tiret, Laurence" uniqKey="Tiret L" first="Laurence" last="Tiret">Laurence Tiret</name>
<affiliation><inist:fA14 i1="10"><s1>INSERM U525, Faculte de Medecin Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Blankenberg, Stefan" sort="Blankenberg, Stefan" uniqKey="Blankenberg S" first="Stefan" last="Blankenberg">Stefan Blankenberg</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">08-0183087</idno>
<date when="2008">2008</date>
<idno type="stanalyst">PASCAL 08-0183087 INIST</idno>
<idno type="RBID">Pascal:08-0183087</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">003665</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary</title>
<author><name sortKey="Macfadyen, Robert J" sort="Macfadyen, Robert J" uniqKey="Macfadyen R" first="Robert J." last="Macfadyen">Robert J. Macfadyen</name>
<affiliation><inist:fA14 i1="01"><s1>University Department of Medicine and Department of Cardiology, City Hospital, Dudley Road</s1>
<s2>Birmingham B18 7QH</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ng Kam Chuen, M Jennyfer" sort="Ng Kam Chuen, M Jennyfer" uniqKey="Ng Kam Chuen M" first="M. Jennyfer" last="Ng Kam Chuen">M. Jennyfer Ng Kam Chuen</name>
<affiliation><inist:fA14 i1="01"><s1>University Department of Medicine and Department of Cardiology, City Hospital, Dudley Road</s1>
<s2>Birmingham B18 7QH</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="West, Malcolm J" sort="West, Malcolm J" uniqKey="West M" first="Malcolm J." last="West">Malcolm J. West</name>
<affiliation><inist:fA14 i1="02"><s1>University of Queensland</s1>
<s2>Brisbane</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Nestel, Paul J" sort="Nestel, Paul J" uniqKey="Nestel P" first="Paul J." last="Nestel">Paul J. Nestel</name>
<affiliation><inist:fA14 i1="03"><s1>Baker Heart Research Institute</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Kirby, Adrienne C" sort="Kirby, Adrienne C" uniqKey="Kirby A" first="Adrienne C." last="Kirby">Adrienne C. Kirby</name>
<affiliation><inist:fA14 i1="04"><s1>NHMRC Clinical Trials Centre, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Schnabel, Renate" sort="Schnabel, Renate" uniqKey="Schnabel R" first="Renate" last="Schnabel">Renate Schnabel</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sullivan, David" sort="Sullivan, David" uniqKey="Sullivan D" first="David" last="Sullivan">David Sullivan</name>
<affiliation><inist:fA14 i1="06"><s1>Royal Prince Alfred Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Simes, R John" sort="Simes, R John" uniqKey="Simes R" first="R. John" last="Simes">R. John Simes</name>
<affiliation><inist:fA14 i1="04"><s1>NHMRC Clinical Trials Centre, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pollicino, Christine" sort="Pollicino, Christine" uniqKey="Pollicino C" first="Christine" last="Pollicino">Christine Pollicino</name>
<affiliation><inist:fA14 i1="04"><s1>NHMRC Clinical Trials Centre, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lubos, Edith" sort="Lubos, Edith" uniqKey="Lubos E" first="Edith" last="Lubos">Edith Lubos</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Munzel, Thomas F" sort="Munzel, Thomas F" uniqKey="Munzel T" first="Thomas F." last="Münzel">Thomas F. Münzel</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="White, Harvey D" sort="White, Harvey D" uniqKey="White H" first="Harvey D." last="White">Harvey D. White</name>
<affiliation><inist:fA14 i1="07"><s1>Green Lane Cardiovascular Service, Auckland City Hospital</s1>
<s2>Auckland</s2>
<s3>NZL</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tonkin, Andrew M" sort="Tonkin, Andrew M" uniqKey="Tonkin A" first="Andrew M." last="Tonkin">Andrew M. Tonkin</name>
<affiliation><inist:fA14 i1="08"><s1>National Heart Foundation</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bickel, Christoph" sort="Bickel, Christoph" uniqKey="Bickel C" first="Christoph" last="Bickel">Christoph Bickel</name>
<affiliation><inist:fA14 i1="09"><s1>Innere Abteilung, Bundeswehrzentralkrankenhaus</s1>
<s2>Koblenz</s2>
<s3>DEU</s3>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tiret, Laurence" sort="Tiret, Laurence" uniqKey="Tiret L" first="Laurence" last="Tiret">Laurence Tiret</name>
<affiliation><inist:fA14 i1="10"><s1>INSERM U525, Faculte de Medecin Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Blankenberg, Stefan" sort="Blankenberg, Stefan" uniqKey="Blankenberg S" first="Stefan" last="Blankenberg">Stefan Blankenberg</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">European heart journal</title>
<title level="j" type="abbreviated">Eur. heart j.</title>
<idno type="ISSN">0195-668X</idno>
<imprint><date when="2008">2008</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">European heart journal</title>
<title level="j" type="abbreviated">Eur. heart j.</title>
<idno type="ISSN">0195-668X</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atherosclerosis</term>
<term>Brain natriuretic peptide</term>
<term>Cardiology</term>
<term>Cardiovascular disease</term>
<term>Circulatory system</term>
<term>Evolution</term>
<term>Fragment</term>
<term>Inhibitor</term>
<term>Level</term>
<term>Lipids</term>
<term>Metalloendopeptidases</term>
<term>Metalloproteinase</term>
<term>N terminal-Sequence</term>
<term>Pravastatin</term>
<term>Prediction</term>
<term>Predictive factor</term>
<term>Predictor</term>
<term>Prognosis</term>
<term>Risk</term>
<term>Risk factor</term>
<term>Tissue</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Pathologie de l'appareil circulatoire</term>
<term>Athérosclérose</term>
<term>Séquence N terminale</term>
<term>Fragment</term>
<term>Peptide BNP</term>
<term>Tissu</term>
<term>Inhibiteur</term>
<term>Metalloendopeptidases</term>
<term>Métalloprotéinase</term>
<term>Niveau</term>
<term>Prédicteur</term>
<term>Facteur prédictif</term>
<term>Prédiction</term>
<term>Pronostic</term>
<term>Evolution</term>
<term>Lipide</term>
<term>Facteur risque</term>
<term>Risque</term>
<term>Pravastatine</term>
<term>Appareil circulatoire</term>
<term>Cardiologie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0195-668X</s0>
</fA01>
<fA03 i2="1"><s0>Eur. heart j.</s0>
</fA03>
<fA05><s2>29</s2>
</fA05>
<fA06><s2>7</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>MACFADYEN (Robert J.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>NG KAM CHUEN (M. Jennyfer)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>WEST (Malcolm J.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="04" i2="1"><s1>NESTEL (Paul J.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="05" i2="1"><s1>KIRBY (Adrienne C.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="06" i2="1"><s1>SCHNABEL (Renate)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="07" i2="1"><s1>SULLIVAN (David)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="08" i2="1"><s1>SIMES (R. John)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="09" i2="1"><s1>POLLICINO (Christine)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="10" i2="1"><s1>LUBOS (Edith)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="11" i2="1"><s1>MÜNZEL (Thomas F.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="12" i2="1"><s1>WHITE (Harvey D.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="13" i2="1"><s1>TONKIN (Andrew M.)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="14" i2="1"><s1>BICKEL (Christoph)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="15" i2="1"><s1>TIRET (Laurence)</s1>
<s9>comment.</s9>
</fA11>
<fA11 i1="16" i2="1"><s1>BLANKENBERG (Stefan)</s1>
<s9>comment.</s9>
</fA11>
<fA14 i1="01"><s1>University Department of Medicine and Department of Cardiology, City Hospital, Dudley Road</s1>
<s2>Birmingham B18 7QH</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>University of Queensland</s1>
<s2>Brisbane</s2>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Baker Heart Research Institute</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>NHMRC Clinical Trials Centre, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1</s1>
<s2>Mainz 55131</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Royal Prince Alfred Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Green Lane Cardiovascular Service, Auckland City Hospital</s1>
<s2>Auckland</s2>
<s3>NZL</s3>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>National Heart Foundation</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Innere Abteilung, Bundeswehrzentralkrankenhaus</s1>
<s2>Koblenz</s2>
<s3>DEU</s3>
<sZ>14 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>INSERM U525, Faculte de Medecin Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA17 i1="01" i2="1"><s1>LIPID Study Investigators</s1>
<s3>INC</s3>
</fA17>
<fA20><s2>837-839, 923-931 [12 p.]</s2>
</fA20>
<fA21><s1>2008</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>18785</s2>
<s5>354000173673100120</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>40 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0183087</s0>
</fA47>
<fA60><s1>P</s1>
<s3>AR</s3>
<s3>CT</s3>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>European heart journal</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B12B01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Pathologie de l'appareil circulatoire</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Cardiovascular disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Athérosclérose</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Atherosclerosis</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Ateroesclerosis</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Séquence N terminale</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>N terminal-Sequence</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Secuencia N terminal</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Fragment</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Fragment</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Fragmento</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Peptide BNP</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Brain natriuretic peptide</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Péptido BNP</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Tissu</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Tissue</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Tejido</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Inhibiteur</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Inhibitor</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Inhibidor</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Metalloendopeptidases</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Metalloendopeptidases</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Metalloendopeptidases</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Métalloprotéinase</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Metalloproteinase</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Metaloproteasa</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Niveau</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Level</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Nivel</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Prédicteur</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Predictor</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Predictor</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Facteur prédictif</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Predictive factor</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Factor predictivo</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Prédiction</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Prediction</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Predicción</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Pronostic</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Prognosis</s0>
<s5>20</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Pronóstico</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Evolution</s0>
<s5>21</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Evolution</s0>
<s5>21</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Evolución</s0>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Lipide</s0>
<s5>22</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>Lipids</s0>
<s5>22</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA"><s0>Lípido</s0>
<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE"><s0>Facteur risque</s0>
<s5>23</s5>
</fC03>
<fC03 i1="17" i2="X" l="ENG"><s0>Risk factor</s0>
<s5>23</s5>
</fC03>
<fC03 i1="17" i2="X" l="SPA"><s0>Factor riesgo</s0>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE"><s0>Risque</s0>
<s5>24</s5>
</fC03>
<fC03 i1="18" i2="X" l="ENG"><s0>Risk</s0>
<s5>24</s5>
</fC03>
<fC03 i1="18" i2="X" l="SPA"><s0>Riesgo</s0>
<s5>24</s5>
</fC03>
<fC03 i1="19" i2="X" l="FRE"><s0>Pravastatine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>25</s5>
</fC03>
<fC03 i1="19" i2="X" l="ENG"><s0>Pravastatin</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>25</s5>
</fC03>
<fC03 i1="19" i2="X" l="SPA"><s0>Pravastatina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>25</s5>
</fC03>
<fC03 i1="20" i2="X" l="FRE"><s0>Appareil circulatoire</s0>
<s5>26</s5>
</fC03>
<fC03 i1="20" i2="X" l="ENG"><s0>Circulatory system</s0>
<s5>26</s5>
</fC03>
<fC03 i1="20" i2="X" l="SPA"><s0>Aparato circulatorio</s0>
<s5>26</s5>
</fC03>
<fC03 i1="21" i2="X" l="FRE"><s0>Cardiologie</s0>
<s5>27</s5>
</fC03>
<fC03 i1="21" i2="X" l="ENG"><s0>Cardiology</s0>
<s5>27</s5>
</fC03>
<fC03 i1="21" i2="X" l="SPA"><s0>Cardiología</s0>
<s5>27</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie des vaisseaux sanguins</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Vascular disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Vaso sanguíneo patología</s0>
<s5>37</s5>
</fC07>
<fN21><s1>112</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 08-0183087 INIST</NO>
<ET>The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary</ET>
<AU>MACFADYEN (Robert J.); NG KAM CHUEN (M. Jennyfer); WEST (Malcolm J.); NESTEL (Paul J.); KIRBY (Adrienne C.); SCHNABEL (Renate); SULLIVAN (David); SIMES (R. John); POLLICINO (Christine); LUBOS (Edith); MÜNZEL (Thomas F.); WHITE (Harvey D.); TONKIN (Andrew M.); BICKEL (Christoph); TIRET (Laurence); BLANKENBERG (Stefan)</AU>
<AF>University Department of Medicine and Department of Cardiology, City Hospital, Dudley Road/Birmingham B18 7QH/Royaume-Uni (1 aut., 2 aut.); University of Queensland/Brisbane/Australie (3 aut.); Baker Heart Research Institute/Melbourne/Australie (4 aut.); NHMRC Clinical Trials Centre, University of Sydney/Sydney/Australie (5 aut., 8 aut., 9 aut.); Department of Medicine II, Johannes Gutenberg University, Langenbeckstr. 1/Mainz 55131/Allemagne (6 aut., 10 aut., 11 aut., 16 aut.); Royal Prince Alfred Hospital/Sydney/Australie (7 aut.); Green Lane Cardiovascular Service, Auckland City Hospital/Auckland/Nouvelle-Zélande (12 aut.); National Heart Foundation/Melbourne/Australie (13 aut.); Innere Abteilung, Bundeswehrzentralkrankenhaus/Koblenz/Allemagne (14 aut.); INSERM U525, Faculte de Medecin Pitie-Salpetriere/Paris/France (15 aut.)</AF>
<DT>Publication en série; Article; Commentaire; Niveau analytique</DT>
<SO>European heart journal; ISSN 0195-668X; Royaume-Uni; Da. 2008; Vol. 29; No. 7; 837-839, 923-931 [12 p.]; Bibl. 40 ref.</SO>
<LA>Anglais</LA>
<EA>Aims We sought to determine the association between two major biomarkers, the inactive N-terminal fragment of brain natriuretic peptide (NT-proBNP) and tissue inhibitor of metalloproteinase-1 (TIMP-1) and long-term cardiovascular outcomes in a cohort of subjects who had a myocardial infarction or unstable angina 3-36 months previously. Methods Plasma NT-proBNP and TIMP-1 were measured in a nested case control study of 250 randomly matched subject and results pairs enrolled in the long-term intervention with pravastatin in ischaemic disease (LIPID) and LIPID extended follow-up studies. Cases (n = 250) were defined as those who had a cardiovascular death, non-fatal myocardial infarction or stroke during the studies. Controls (n = 250) remained event-free for the same follow-up duration (average 2.5 years) as the matched cases. The relationships between cases and plasma NT-proBNP and TIMP-1 were adjusted for the LIPID risk score, treatment allocation and other biomarkers (CRP, IL-6 and white cell count), and examined using a multivariable conditional logistic regression model. NT-proBNP levels were significantly higher in the cases than in the controls [389 (152-864) vs. 198 (93-416) pg/mL, median (25%-75% percentiles), P< 0.001]. The odds ratio (OR) of recurrent cardiovascular events in individuals in the highest quartile was three times higher than those in the lowest quartile (95% confidence interval (Cl) 1.8-5.1; P < 0.001). Similarly, TIMP-1 levels were significantly higher among cases compared with controls (806 vs. 736 pg/mL, median: highest vs. lowest quartile: OR 2.8, 95% Cl 1.6-4.7; P < 0.001). After adjustment for the LIPID risk score, treatment with pravastatin and other biomarkers, both NT-proBNP and TIMP-1 predicted cardiovascular events significantly and independently of each other. Conclusion The study suggests that in subjects with stable ischaemic disease, NT-proBNP and TIMP-1 are independent predictive markers of coronary heart disease outcome.</EA>
<CC>002B12B01</CC>
<FD>Pathologie de l'appareil circulatoire; Athérosclérose; Séquence N terminale; Fragment; Peptide BNP; Tissu; Inhibiteur; Metalloendopeptidases; Métalloprotéinase; Niveau; Prédicteur; Facteur prédictif; Prédiction; Pronostic; Evolution; Lipide; Facteur risque; Risque; Pravastatine; Appareil circulatoire; Cardiologie</FD>
<FG>Peptidases; Hydrolases; Enzyme; Pathologie des vaisseaux sanguins</FG>
<ED>Cardiovascular disease; Atherosclerosis; N terminal-Sequence; Fragment; Brain natriuretic peptide; Tissue; Inhibitor; Metalloendopeptidases; Metalloproteinase; Level; Predictor; Predictive factor; Prediction; Prognosis; Evolution; Lipids; Risk factor; Risk; Pravastatin; Circulatory system; Cardiology</ED>
<EG>Peptidases; Hydrolases; Enzyme; Vascular disease</EG>
<SD>Aparato circulatorio patología; Ateroesclerosis; Secuencia N terminal; Fragmento; Péptido BNP; Tejido; Inhibidor; Metalloendopeptidases; Metaloproteasa; Nivel; Predictor; Factor predictivo; Predicción; Pronóstico; Evolución; Lípido; Factor riesgo; Riesgo; Pravastatina; Aparato circulatorio; Cardiología</SD>
<LO>INIST-18785.354000173673100120</LO>
<ID>08-0183087</ID>
</server>
</inist>
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The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary

The value of N-terminal fragment of brain natriuretic peptide and tissue inhibitor of metalloproteinase-1 levels as predictors of cardiovascular outcome in the LIPID study. Commentary

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